Chapter 13. Memory, Learning, and Development
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By Maggie Fox Teenagers who use marijuana heavily grow up to have poor memories and also have brain abnormalities, a new study shows. The study cannot say which came first — the brain structure differences or the pot use. But it suggests there could be long-term effects of heavy marijuana use. A team at Northwestern University looked at 97 volunteers with and without mental illness. The dope smokers said they'd used marijuana daily starting at age 16 or 17, and said they had not used other drugs. The daily marijuana users had an abnormally shaped hippocampus and performed about 18 percent more poorly on long-term memory tasks, the researchers reported in the journal Hippocampus. The hippocampus is a part of the brain used in storing long-term memory. "The memory processes that appear to be affected by cannabis are ones that we use every day to solve common problems and to sustain our relationships with friends and family," said Dr. John Csernansky, who worked on the study. Previous research by the same Northwestern team showed heavy pot smokers had poor short-term and working memory and abnormally shaped brain structures including the striatum, globus pallidus and thalamus. "It is possible that the abnormal brain structures reveal a pre-existing vulnerability to marijuana abuse," Matthew Smith, who led the study, said in a statement.
By Emily Underwood From imaging babies to blasting apart kidney stones, ultrasound has proved to be a versatile tool for physicians. Now, several research teams aim to unleash the technology on some of the most feared brain diseases. The blood-brain barrier, a tightly packed layer of cells that lines the brain's blood vessels, protects it from infections, toxins, and other threats but makes the organ frustratingly hard to treat. A strategy that combines ultrasound with microscopic blood-borne bubbles can briefly open the barrier, in theory giving drugs or the immune system access to the brain. In the clinic and the lab, that promise is being evaluated. This month, in one of the first clinical tests, Todd Mainprize, a neurosurgeon at the University of Toronto in Canada, hopes to use ultrasound to deliver a dose of chemotherapy to a malignant brain tumor. And in some of the most dramatic evidence of the technique's potential, a research team reports this week in Science Translational Medicine that they used it to rid mice of abnormal brain clumps similar to those in Alzheimer's disease, restoring lost memory and cognitive functions. If such findings can be translated from mice to humans, “it will revolutionize the way we treat brain disease,” says biophysicist Kullervo Hynynen of the Sunnybrook Research Institute in Toronto, who originated the ultrasound method. Some scientists stress that rodent findings can be hard to translate to humans and caution that there are safety concerns about zapping the brain with even the low-intensity ultrasound used in the new study, which is similar to that used in diagnostic scans. © 2015 American Association for the Advancement of Science.
Link ID: 20685 - Posted: 03.12.2015
|By Daisy Yuhas The brain is a hotbed of electrical activity. Scientists have long known that brain cells communicate via electrical missives, created by charged atoms and molecules called ions as they travel across the membranes of those cells. But a new study suggests that in the days and weeks that lead up to a brain forming in an embryo or fetus, altering the electrical properties of these cells can dramatically change how the ensuing brain develops. Researchers at Tufts University and the University of Minnesota have investigated how the difference in charge on either side of a resting cell’s membrane—its electrical potential—helps build the brain. In previous work Tufts University developmental biologist Michael Levin found that patterns of electrical potentials in the earliest stages of an embryo’s development can direct how an animal’s body grows, and that manipulating those potentials can cause a creature to sprout extra limbs, tails or functioning eyes. Now, Levin’s group has investigated how these potentials shape the brain. Working with frog embryos the researchers first used dyes to see the patterns of electrical potentials that precede brain development. They noticed that before the development of a normal brain the cells lining the neural tube, a structure that eventually becomes the brain and spinal cord, have extreme differences in ionic charge within and outside the membrane that houses the cells. In other words, these cells are extremely polarized. © 2015 Scientific American
Keyword: Development of the Brain
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Older people could improve or maintain their mental function through heart healthy lifestyle changes, a large randomized trial for dementia prevention shows. Researchers in Finland and Sweden designed a trial to tackle risk factors for Alzheimer's disease. The 1,260 Finns aged 60 to 77 participating in the study were all considered at risk of dementia based on standard test scores. Half were randomly assigned to receive advice from health professionals on maintaining a healthy diet, aerobic and muscle training exercises, brain training exercises and regular checks of blood pressure, height and weight for body mass index and physical exams for two years or regular health advice. Participants in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability or FINGER study had their cognitive function measured in a battery of mental tests. "The main hypothesis was that simultaneous changes in several risk factors (even of smaller magnitude) would lead to a protective effect on cognition," Miia Kivipelto from the Karolinska Institute in Stockholm and her co-authors said in Wednesday's issue of The Lancet. Overall, test scores were 25 per cent in the diet and training group than the control group. There was no effect on memory. ©2015 CBC/Radio-Canada.
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Mutations in the presenilin-1 gene are the most common cause of inherited, early-onset forms of Alzheimer’s disease. In a new study, published in Neuron, scientists replaced the normal mouse presenilin-1 gene with Alzheimer’s-causing forms of the human gene to discover how these genetic changes may lead to the disorder. Their surprising results may transform the way scientists design drugs that target these mutations to treat inherited or familial Alzheimer’s, a rare form of the disease that affects approximately 1 percent of people with the disorder. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For decades, it has been unclear exactly how the presenilin mutations cause Alzheimer’s disease. Presenilin is a component of an important enzyme, gamma secretase, which cuts up amyloid precursor protein into two protein fragments, Abeta40 and Abeta42. Abeta42 is found in plaques, the abnormal accumulations of protein in the brain which are a hallmark of Alzheimer’s. Numerous studies suggested that presenilin-1 mutations increased activity of gamma-secretase. Investigators have developed drugs that block gamma-secretase, but they have so far failed in clinical trials to halt the disease. The study led by Raymond Kelleher, M.D., Ph.D. and Jie Shen, Ph.D., professors of neurology at Harvard Medical School, Boston, provides a plot twist in the association of presenilin-1 mutations and inherited Alzheimer’s disease. Using mice with altered forms of the presenilin gene, Drs. Kelleher and Shen discovered that the mutations may cause the disease by decreasing, rather than increasing, the activity of gamma-secretase.
|By Esther Landhuis As we age, we seem to get worse at ignoring irrelevant stimuli. It's what makes restaurant conversations challenging—having to converse while also shutting out surrounding chatter. New research bears out the aging brain's distractibility but also suggests that training may help us tune out interference. Scientists at Brown University recruited seniors and twentysomethings for a visual experiment. Presented with a sequence of letters and numbers, participants were asked to report back only the numbers—all the while disregarding a series of meaningless dots. Sometimes the dots moved randomly, but other times they traveled in a clear direction, making them harder to ignore. Older participants ended up accidentally learning the dots' patterns, based on the accuracy of their answers when asked which way the dots were moving, whereas young adults seemed able to suppress that information and focus on the numbers, the researchers reported last November in Current Biology. In a separate study published in Neuron, scientists at the University of California, San Francisco, showed they could train aging brains to become less distractible. Their regimen helped aging rats as well as older people. The researchers played three different sounds and rewarded trainees for identifying a target tone while ignoring distracter frequencies. As the subjects improved, the task grew more challenging—the distracting tone became harder to discriminate from the target. © 2015 Scientific American,
By Douglas Starr In 1906, Hugo Münsterberg, the chair of the psychology laboratory at Harvard University and the president of the American Psychological Association, wrote in the Times Magazine about a case of false confession. A woman had been found dead in Chicago, garroted with a copper wire and left in a barnyard, and the simpleminded farmer’s son who had discovered her body stood accused. The young man had an alibi, but after questioning by police he admitted to the murder. He did not simply confess, Münsterberg wrote; “he was quite willing to repeat his confession again and again. Each time it became richer in detail.” The young man’s account, he continued, was “absurd and contradictory,” a clear instance of “the involuntary elaboration of a suggestion” from his interrogators. Münsterberg cited the Salem witch trials, in which similarly vulnerable people were coerced into self-incrimination. He shared his opinion in a letter to a Chicago nerve specialist, which made the local press. A week later, the farmer’s son was hanged. Münsterberg was ahead of his time. It would be decades before the legal and psychological communities began to understand how powerfully suggestion can shape memory and, in turn, the course of justice. In the early nineteen-nineties, American society was recuperating from another panic over occult influence; Satanists had replaced witches. One case, the McMartin Preschool trial, hinged on nine young victims’ memories of molestation and ritual abuse—memories that they had supposedly forgotten and then, after being interviewed, recovered. The case fell apart, in 1990, because the prosecution could produce no persuasive evidence of the victims’ claims. A cognitive psychologist named Elizabeth Loftus, who had consulted on the case, wondered whether the children’s memories might have been fabricated—in Münsterberg’s formulation, involuntarily elaborated—rather than actually recovered.
Keyword: Learning & Memory
Link ID: 20679 - Posted: 03.12.2015
Mo Costandi Neuroscientists in France have implanted false memories into the brains of sleeping mice. Using electrodes to directly stimulate and record the activity of nerve cells, they created artificial associative memories that persisted while the animals snoozed and then influenced their behaviour when they awoke. Manipulating memories by tinkering with brain cells is becoming routine in neuroscience labs. Last year, one team of researchers used a technique called optogenetics to label the cells encoding fearful memories in the mouse brain and to switch the memories on and off, and another used it to identify the cells encoding positive and negative emotional memories, so that they could convert positive memories into negative ones, and vice versa. The new work, published today in the journal Nature Neuroscience, shows for the first time that artificial memories can be implanted into the brains of sleeping animals. It also provides more details about how populations of nerve cells encode spatial memories, and about the important role that sleep plays in making such memories stronger. Karim Benchenane of the French National Centre for Scientific Research (CNRS) in Paris and his colleagues implanted electrodes into the brains of 40 mice, targeting the medial forebrain bundle (MFB), a component of the reward circuitry, and the CA1 region of the hippocampus, which contains at least three different cell types that encode the memories needed for spatial navigation. © 2015 Guardian News and Media Limited
By Rachel Rabkin Peachman Many women with a history of depression who take antidepressants assume that once they get pregnant, they should try to wean themselves off their meds to avoid negative side effects for the baby. A new large study published in the journal Pediatrics challenges one reason behind that assumption. The research found that taking selective serotonin reuptake inhibitors (the antidepressants also known as S.S.R.I.s) while pregnant does not increase the risk of asthma in the resulting babies. What is associated with an increased risk of asthma? According to this study and other research, untreated prenatal depression. “The mechanisms underlying the association of prenatal depression and asthma are unknown,” said Dr. Xiaoqin Liu, the lead author of the Pediatrics study and an epidemiologist at Aarhus University in Denmark. An association between prenatal depression and asthma does not mean that prenatal depression causes asthma. There could be other reasons for the correlation, genetic or environmental, or both. For example, people who live in dense, polluted urban areas could be at an increased risk of both asthma and depression. The researchers used Denmark’s national registries to evaluate all singleton babies born from 1996 to 2007, and identify the mothers who had a diagnosis of depression or had used antidepressants, or both, during pregnancy or one year beforehand. Using a statistical model, the study authors found that prenatal depression — with or without the use of antidepressants — was associated with a 25 percent increased risk of asthma in children as compared with children whose mothers did not have a record of depression. © 2015 The New York Times Company
by Penny Sarchet For some of us, it might have been behind the bikeshed. Not so the African cotton leafworm moth (Spodoptera littoralis), which can choose any one of a vast number of plant species to mate on. But these moths remember their first time, returning to the same species in search of other mates. In the wild, this moth feeds and mates on species from as many as 40 different plant families. That much choice means there's usually something available to eat, but selecting and remembering the best plants is tricky. So, recalling what you ate as a larva, or where you first copulated, may help narrow down which plants provide better quality food or are more likely to attract other potential mates. Magali Proffit and David Carrasco of the Swedish University of Agricultural Sciences in Alnarp and their colleagues have discovered that this moth's first mating experience shapes its future preferences. These moths have an innate preference for cotton plants over cabbage. But when the researchers made them mate for the first time on cabbage, the moths later showed an increased preference for mating or laying eggs on this plant. Further experiments revealed that moths didn't just favour plants they were familiar with, even in combination with a sex pheromone – mating had to be involved. © Copyright Reed Business Information Ltd.
By Will Boggs MD NEW YORK (Reuters Health) - Adolescents with a history of childhood trauma show different neural responses to subjective anxiety and craving, researchers report. "I think the finding of increased activation of insula, anterior cingulate, and prefrontal cortex in response to stress cues in the high- relative to low-trauma group, while arguably not necessarily unexpected, is important as it suggests that youth exposed to higher levels of trauma may experience different brain responses to similar stressors," Dr. Marc N. Potenza from Yale University, New Haven, Connecticut told Reuters Health by email. Childhood trauma has been associated with anxiety and depression, as well as obesity, risky sexual behavior, and substance use. Previous imaging studies have not investigated neural responses to personalized stimuli, Dr. Potenza and his colleagues write in Neuropsychopharmacology, online January 8. The team used functional MRI to assess regional brain activations to personalized appetitive (favorite food), aversive (stress), and neutral/relaxing cues in 64 adolescents, including 33 in the low-trauma group and 31 in the high-trauma group. Two-thirds of the adolescents had been exposed to cocaine prenatally, with prenatal cocaine exposure being significantly over-represented in the high-trauma group. Compared with the low-trauma group, the high-trauma group showed increased responsivity in several cortical regions in response to stress, as well as decreased activation in the cerebellar vermis and right cerebellum in response to neutral/relaxing cues. But the two groups did not differ significantly in their responses to favorite-food cues, the researchers found. © 2015 Scientific American
Children who attend school in heavy traffic areas may show slower cognitive development and lower memory test scores, Spanish researchers have found. About 21,000 premature deaths are attributed to air pollution in Canada each year, according to the Canadian Medical Association. The detrimental effects of air pollution on cardiovascular health and on the lungs are well documented and now researchers are looking at its effects on the brain. To that end, Dr. Jordi Sunyer and his colleagues from the Centre for Research in Environmental Epidemiology in Barcelona measured three aspects of memory and attentiveness in more than 2,700 primary school children every three months over 12 months. "What was surprising for us is among our children, we see very robust, consistent effects," Sunyer said Tuesday from Rome. The associations between slower cognitive development and higher levels of air pollutants remained after the researchers took factors such as parents’ education, commuting time, smoking in the home and green spaces at school into account. The researchers measured air pollutants from traffic twice, in the school courtyard and inside the classroom for schools with high and low traffic-related air pollution. Pollutants from burning fossil fuels, carbon, nitrogen dioxide and ultrafine particles were measured. For example, working memory improved 7.4 per cent among children in highly polluted schools compared with 11.5 per cent among those in less polluted schools. ©2015 CBC/Radio-Canada.
Lights, sound, action: we are constantly learning how to incorporate outside sensations into our reactions in specific situations. In a new study, brain scientists have mapped changes in communication between nerve cells as rats learned to make specific decisions in response to particular sounds. The team then used this map to accurately predict the rats’ reactions. These results add to our understanding of how the brain processes sensations and forms memories to inform behavior. “We’re reading the memories in the brain,” said Anthony Zador, M.D., Ph.D., professor at Cold Spring Harbor Laboratory, New York, and senior author of the study, published in Nature. The work was funded by the National Institutes of Health and led by Qiaojie Xiong, Ph.D., a former postdoctoral researcher in Dr. Zador’s laboratory. “For decades scientists have been trying to map memories in the brain,” said James Gnadt, Ph.D., a program director at the National Institute of Neurological Disorders and Stroke (NINDS), one of the NIH institutes that funded the study. “This study shows that scientists can begin to pinpoint the precise synapses where certain memories form and learning occurs.” The communication points, or synapses, that Dr. Zador’s lab studied were in the striatum, an integrating center located deep inside the brain that is known to play an important role in coordinating the translation of thoughts and sensations into actions. Problems with striatal function are associated with certain neurological disorders such as Huntington’s disease in which affected individuals have severely impaired skill learning.
By Nicholas Bakalar Gout, a form of arthritis, is extremely painful and associated with an increased risk for cardiovascular problems. But there is a bright side: It may be linked to a reduced risk for Alzheimer’s disease. Researchers compared 59,204 British men and women with gout to 238,805 without the ailment, with an average age of 65. Patients were matched for sex, B.M.I., smoking, alcohol consumption and other characteristics. The study, in The Annals of the Rheumatic Diseases, followed the patients for five years. They found 309 cases of Alzheimer’s among those with gout and 1,942 among those without. Those with gout, whether they were being treated for the condition or not, had a 24 percent lower risk of Alzheimer’s disease. The reason for the connection is unclear. But gout is caused by excessive levels of uric acid in the blood, and previous studies have suggested that uric acid protects against oxidative stress. This may play a role in limiting neuron degeneration. “This is a dilemma, because uric acid is thought to be bad, associated with heart disease and stroke,” said the senior author, Dr. Hyon K. Choi, a professor of medicine at Harvard. “This is the first piece of data suggesting that uric acid isn’t all bad. Maybe there is some benefit. It has to be confirmed in randomized trials, but that’s the interesting twist in this story.” © 2015 The New York Times Company
By Roni Caryn Rabin When my mother, Pauline, was 70, she lost her sense of balance. She started walking with an odd shuffling gait, taking short steps and barely lifting her feet off the ground. She often took my hand, holding it and squeezing my fingers. Her decline was precipitous. She fell repeatedly. She stopped driving, and she could no longer ride her bike in a straight line along the C&O Canal. The woman who taught me the sidestroke couldn’t even stand in the shallow end of the pool. “I feel like I’m drowning,” she’d say. A retired psychiatrist, my mother had numerous advantages — education, resources and insurance — but, still, getting the right diagnosis took nearly 10 years. Each expert saw the problem through the narrow prism of a single specialty. Surgeons recommended surgery. Neurologists screened for common incurable conditions. The answer was under their noses, in my mother’s hunches and her family history. But it took a long time before someone connected the dots. My mother was using a walker by the time she was told she had a rare condition that causes gait problems and cognitive loss, and is one of the few treatable forms of dementia. The bad news was that it had taken so long to get the diagnosis that some of the damage might not be reversible. “This should be one of the first things physicians look for in an older person,” my mother said recently. “You can actually do something about it.”
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By ROBERT PEAR WASHINGTON — Federal investigators say they have found evidence of widespread overuse of psychiatric drugs by older Americans with Alzheimer’s disease, and are recommending that Medicare officials take immediate action to reduce unnecessary prescriptions. The findings will be released Monday by the Government Accountability Office, an arm of Congress, and come as the Obama administration has already been working with nursing homes to reduce the inappropriate use of antipsychotic medications like Abilify, Risperdal, Zyprexa and clozapine. But in the study, investigators said officials also needed to focus on overuse of such drugs by people with dementia who live at home or in assisted living facilities. The Department of Health and Human Services “has taken little action” to reduce the use of antipsychotic drugs by older adults living outside nursing homes, the report said. Doctors sometimes prescribe antipsychotic drugs to calm patients with dementia who display disruptive behavior like hitting, yelling or screaming, the report said. Researchers said this was often the case in nursing homes that had inadequate numbers of employees. Dementia is most commonly associated with a decline in memory, but doctors say it can also cause changes in mood or personality and, at times, agitation or aggression. Experts have raised concern about the use of antipsychotic drugs to address behavioral symptoms of Alzheimer’s and other forms of dementia. The Food and Drug Administration says antipsychotic drugs are often associated with an increased risk of death when used to treat older adults with dementia who also have psychosis. © 2015 The New York Times Company
By Elizabeth Pennisi Last week, researchers expanded the size of the mouse brain by giving rodents a piece of human DNA. Now another team has topped that feat, pinpointing a human gene that not only grows the mouse brain but also gives it the distinctive folds found in primate brains. The work suggests that scientists are finally beginning to unravel some of the evolutionary steps that boosted the cognitive powers of our species. “This study represents a major milestone in our understanding of the developmental emergence of human uniqueness,” says Victor Borrell Franco, a neurobiologist at the Institute of Neurosciences in Alicante, Spain, who was not involved with the work. The new study began when Wieland Huttner, a developmental neurobiologist at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany, and his colleagues started closely examining aborted human fetal tissue and embryonic mice. “We specifically wanted to figure out which genes are active during the development of the cortex, the part of the brain that is greatly expanded in humans and other primates compared to rodents,” says Marta Florio, the Huttner graduate student who carried out the main part of the work. That was harder than it sounded. Building a cortex requires several kinds of starting cells, or stem cells. The stem cells divide and sometimes specialize into other types of “intermediate” stem cells that in turn divide and form the neurons that make up brain tissue. To learn what genes are active in the two species, the team first had to develop a way to separate out the various types of cortical stem cells. © 2015 American Association for the Advancement of Science
Elizabeth Gibney DeepMind, the Google-owned artificial-intelligence company, has revealed how it created a single computer algorithm that can learn how to play 49 different arcade games, including the 1970s classics Pong and Space Invaders. In more than half of those games, the computer became skilled enough to beat a professional human player. The algorithm — which has generated a buzz since publication of a preliminary version in 2013 (V. Mnih et al. Preprint at http://arxiv.org/abs/1312.5602; 2013) — is the first artificial-intelligence (AI) system that can learn a variety of tasks from scratch given only the same, minimal starting information. “The fact that you have one system that can learn several games, without any tweaking from game to game, is surprising and pretty impressive,” says Nathan Sprague, a machine-learning scientist at James Madison University in Harrisonburg, Virginia. DeepMind, which is based in London, says that the brain-inspired system could also provide insights into human intelligence. “Neuroscientists are studying intelligence and decision-making, and here’s a very clean test bed for those ideas,” says Demis Hassabis, co-founder of DeepMind. He and his colleagues describe the gaming algorithm in a paper published this week (V. Mnih et al. Nature 518, 529–533; 2015. Games are to AI researchers what fruit flies are to biology — a stripped-back system in which to test theories, says Richard Sutton, a computer scientist who studies reinforcement learning at the University of Alberta in Edmonton, Canada. “Understanding the mind is an incredibly difficult problem, but games allow you to break it down into parts that you can study,” he says. But so far, most human-beating computers — such as IBM’s Deep Blue, which beat chess world champion Garry Kasparov in 1997, and the recently unveiled algorithm that plays Texas Hold ’Em poker essentially perfectly (see Nature http://doi.org/2dw; 2015)—excel at only one game. © 2015 Nature Publishing Group
By DENISE GRADY Faced with mounting evidence that general anesthesia may impair brain development in babies and young children, experts said Wednesday that more research is greatly needed and that when planning surgery for a child, parents and doctors should consider how urgently it is required, particularly in children younger than 3 years. In the United States each year, about a million children younger than 4 have surgery with general anesthesia, according to the Food and Drug Administration. So far, the threat is only a potential one; there is no proof that children have been harmed. The concern is based on two types of research. Experiments in young monkeys and other animals have shown that commonly used anesthetics and sedatives can kill brain cells, diminish learning and memory and cause behavior problems. And studies in children have found an association between learning problems and multiple exposures to anesthesia early in life — though not single exposures. But monkeys are not humans, and association does not prove cause and effect. Research now underway is expected to be more definitive, but results will not be available for several years. Anesthesiologists and surgeons are struggling with how — and sometimes whether — to explain a theoretical hazard to parents who are already worried about the real risks of their child’s medical problem and the surgery needed to correct it. If there is a problem with anesthesia, in many cases it may be unavoidable because there are no substitute drugs. The last thing doctors want to do is frighten parents for no reason or prompt them to delay or cancel an operation that their child needs. “On the one hand, we don’t want to overstate the risk, because we don’t know what the risk is, if there is a risk,” said Dr. Randall P. Flick, a pediatric anesthesiologist and director of Mayo Clinic Children’s Center in Rochester, Minn., who has conducted some of the studies in children suggesting a link to learning problems. “On the other hand, we want to make people aware of the risk because we feel we have a duty to do so.” © 2015 The New York Times Compan
By Michelle Roberts Health editor, BBC News online Scientists have proposed a new idea for detecting brain conditions including Alzheimer's - a skin test. Their work, which is at an early stage, found the same abnormal proteins that accumulate in the brain in such disorders can also be found in skin. Early diagnosis is key to preventing the loss of brain tissue in dementia, which can go undetected for years. But experts said even more advanced tests, including ones of spinal fluid, were still not ready for clinic. If they were, then doctors could treatment at the earliest stages, before irreversible brain damage or mental decline has taken place. Brain biomarker Investigators have been hunting for suitable biomarkers in the body - molecules in blood or exhaled breath, for example, that can be measured to accurately and reliably signal if a disease or disorder is present. Dr Ildefonso Rodriguez-Leyva and colleagues from the University of San Luis Potosi, Mexico, believe skin is a good candidate for uncovering hidden brain disorders. Skin has the same origin as brain tissue in the developing embryo and might, therefore, be a good window to what's going on in the mind in later life - at least at a molecular level - they reasoned. Post-mortem studies of people with Parkinson's also reveal that the same protein deposits which occur in the brain with this condition also accumulate in the skin. To test if the same was true in life as after death, the researchers recruited 65 volunteers - 12 who were healthy controls and the remaining 53 who had either Parkinson's disease, Alzheimer's or another type of dementia. They took a small skin biopsy from behind the ear of each volunteer to test in their laboratory for any telltale signs of disease. Specifically, they looked for the presence of two proteins - tau and alpha-synuclein. © 2015 BBC.